The role of genomic islands in Escherichia coli K1 interactions with intestinal and kidney epithelial cells
The completion of Escherichia coli K1 genome has identified several genomic islands that are present in meningitis-causing E. coli RS218 but absent in the non-pathogenic E. coli MG1655. In this study, the role of various genomic islands in E. coli K1 interactions with intestinal epithelial cells (...
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Main Authors: | , , , |
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Format: | Article |
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Elsevier
2016
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Online Access: | http://eprints.sunway.edu.my/624/ http://dx.doi.org/10.1016/j.micpath.2016.02.002 |
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Summary: | The completion of Escherichia coli K1 genome has identified several genomic islands that are present in
meningitis-causing E. coli RS218 but absent in the non-pathogenic E. coli MG1655. In this study, the role
of various genomic islands in E. coli K1 interactions with intestinal epithelial cells (Caco-2) and kidney
epithelial cells (MA104) was determined. Using association assays, invasion assays, and intracellular
survival assays, the findings revealed that the genomic island deletion mutants of RS218 related to P
fimbriae, S fimbriae, F17-like fimbriae, non-fimbrial adhesins, Hek and hemagglutinin, protein secretion
system (T1SS for hemolysin; T2SS; T5SS for antigen 43), Iro system and hmu system), invasins (CNF1,
IbeA), toxins (a-hemolysin), K1 capsule biosynthesis, metabolism (D-serine catabolism, dihydroxyacetone,
glycerol, and glyoxylate metabolism), prophage genes, showed reduced interactions with both cell
types. Next, we determined the role of various genomic islands in E. coli K1 resistance to serum. When
exposed to the normal human serum, the viability of the genomic island deletion mutants related to
adhesins such as S fimbriae, P fimbriae, F17-like fimbriae, non-fimbrial adhesins, Hek and hemagglutinin,
antigen 43 and T5SS for antigen 43, T2SS, and T1SS for hemolysin, Iro system and hmu system, prophage
genes, metabolism (sugar metabolism and D-serine catabolism), K1 capsule biosynthesis, and invasins
such as CNF1 was affected, suggesting their role in bacteremia. The characterization of these genomic
islands should reveal mechanisms of E. coli K1 pathogenicity that could be of value as therapeutic targets. |
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